Background — Benefits of moderate endurance training include increases in parasympathetic activity and baroreflex sensitivity (BRS) and a relative decrease in sympathetic tone. However, the effect of very intensive training load on neural cardiovascular regulation is not known. We tested the hypothesis that strenuous endurance training, like in high-performance athletes, would enhance sympathetic activation and reduce vagal inhibition. Methods and Results — We studied the entire Italian junior national team of rowing (n=7) at increasing training loads up to 75% and 100% of maximum, the latter ∼20 days before the Rowing World Championship. Autoregressive power spectral analysis was used to investigate RR interval and blood pressure (BP) variabilities. BRS was assessed by the sequences method. Increasing training load up to 75% of maximum was associated with a progressive resting bradycardia and increased indexes of cardiac vagal modulation and BRS. However, at 100% training load these effects were reversed, with increases in resting heart rate, diastolic BP, low-frequency RR interval, and BP variabilities and decreases in high-frequency RR variability and BRS. Three athletes later won medals in the World Championship. Conclusions — This study indicates that very intensive endurance training shifted the cardiovascular autonomic modulation from a parasympathetic toward a sympathetic predominance. This finding should be interpreted within the context of the substantial role played by the sympathetic nervous system in increasing cardiovascular performance at peak training. Whether the altered BP and autonomic function shown in this study might be in time hazardous to human cardiovascular system remains to be established.

Background —Myocardial ischemia and infarction impair baroreflex sensitivity (BRS), which when depressed is predictive of future cardiac events after myocardial infarction (MI). The main objective of this study was to determine whether exercise training improves BRS in patients with coronary artery disease. Methods and Results —Ninety-seven male patients with and without a previous MI were recruited after myocardial revascularization surgery and randomized into trained (TR) or untrained (UTR) groups. TR patients underwent a residential exercise program at 85% of maximum heart rate (HRmax) consisting of 2 daily sessions 6 times a week for 2 weeks. Eighty-six patients (45 TR and 41 UTR) completed the study. BRS was assessed at baseline and at the end of the protocol by the spontaneous baroreflex method. The standard deviation of mean R-R interval (RRSD) was also assessed as a measure of heart rate variability. At baseline, there were no significant differences between TR and UTR patients in any variable. In TR patients, BRS increased from 3.0±0.3 to 5.3±0.7 ms/mm Hg ( P <0.001), RRSD from 18.7±1.4 to 23.6±1.6 ms ( P <0.01), and R-R interval from 792.0±15.5 to 851.3±20.5 ms ( P <0.001). No significant changes occurred in UTR patients. Increases in BRS and RRSD were significant in patients either with or without a previous MI. Conclusions —Exercise training increases BRS and heart rate variability in patients with coronary artery disease. Improved cardiac autonomic function might add to the other benefits of exercise training in secondary prevention of ischemic heart disease.

Background —It is currently assumed that during static exercise, central command increases heart rate (HR) through a decrease in parasympathetic activity, whereas the muscle metaboreflex raises blood pressure (BP) only through an increase in sympathetic outflow to blood vessels, because when the metaboreflex activation is maintained during postexercise muscle ischemia, BP remains elevated while HR recovers. We tested the hypotheses that the muscle metaboreflex contributes to HR regulation during static exercise via sympathetic activation and that the arterial baroreflex is involved in the HR recovery of postexercise muscle ischemia. Methods and Results —Eleven healthy male volunteers performed 4-minute static leg extension (SLE) at 30% of maximal voluntary contraction, followed by 4-minute arrested leg circulation (ALC). Autonomic regulation of HR was investigated by spectral analysis of HR variability (HRV), and baroreflex control of heart period was assessed by the spontaneous baroreflex method. SLE resulted in a significant increase in the low-frequency component of HRV that remained elevated during ALC. The normalized high-frequency component of HRV was reduced during SLE and returned to control levels during ALC. Baroreflex sensitivity was significantly reduced during SLE and returned to control levels during ALC when BP was kept elevated above the resting level while HR recovered. Conclusions —The muscle metaboreflex contributes to HR regulation during static exercise via a sympathetic activation. The bradycardia that occurs during postexercise muscle ischemia despite the maintained sympathetic stimulus may be explained by a baroreflex-mediated increase in parasympathetic outflow to the sinoatrial node that overpowers the metaboreflex-induced cardiac sympathetic activation.

Ctors could result in a better quantification of training responses and performance in LDR in comparison to methods on the basis of average-based group values. Methods: The training load responses of eight LDR (aged 39.9 ± 6.5 yr) were monitored using a modified version of the average-based TRIMP called individualized TRIMP (TRIMPi) during a period of 8 wk. The TRIMPi was determined in each LDR using individual HR and lactate profiles determined during an incremental treadmill test. Training-induced effects on performance (5- and 10-km races) and changes in submaximal aerobic fitness (speeds at selected blood lactate concentrations of 2 and 4 mmol·L−1) were assessed before and at the end of the training intervention. Results: Speed at 2 mmol·L−1 (+21.3 ± 5.2%, P < 0.001) and 4 mmol·L−1 (+10.6 ± 2.4%, P < 0.01) concentrations significantly increased after training. Improvements in running speed (%) at 2 mmol·L−1 (r = 0.87, P = 0.005) and 4 mmol·L−1 (r = 0.74, P = 0.04) concentrations were significantly related to weekly TRIMPi sum. No significant relationship between any variable was detected when average-based group values were used. The TRIMPi was significantly related to 5000- (r = −0.77; P = 0.02) and 10,000-m track performances (r = −0.82; P = 0.01). Conclusions: Individualized TRIMP is a valid tool in tracking fitness (speed at 2 and 4 mmol·L−1) and performance (i.e., 5000- and 10,000-m races) in LDR and is more valuable than the methods on the basis of average-based group values. TRIMPi could predict race performance in LDR....